Oropharyngeal Dysphagia after Stroke: Incidence, Diagnosis,

and Clinical Predictors in Patients Admitted to

a Neurorehabilitation Unit

Paolo Falsetti, MD, PhD,* Caterina Acciai, MD, PhD,* Rosanna Palilla, MD,*
Marco Bosi, MD,† Francesco Carpinteri, MD,* Alberto Zingarelli, MD,†
Claudio Pedace, MD,‡ and Lucia Lenzi, MD*

Objective: We analyzed patients with stroke in a neurorehabilitation unit to define

incidence of dysphagia, compare clinical bedside assessment and videofluoroscopy
(VFS), and define any correlation between dysphagia and clinical characteristic of
patients. Methods: In all, 151 consecutive inpatients with recent ischemic or hemor-
rhagic stroke were enrolled. Results: Dysphagia was clinically diagnosed in 62 of 151
patients (41%). A total of 49 patients (79% of clinically dysphagic patients) under-
went VFS. Six patients clinically suggested to be dysphagic had a normal VFS find-
ing. The correlation between clinical and VFS diagnosis of dysphagia was significant (r
5 0.6505). Penetrations and aspirations were observed, respectively, in 42.8% and
26.5% of patients with dysphagia, with 12.2% classified as silent. Lower respiratory
tract infections were observed in 5.9%, more frequently in patients with dysphagia
(30%). Dysphagia was not influenced by type of stroke. Cortical stroke of nondominant
side was associated with dysphagia (P 5 .0322) and subcortical nondominant stroke
showed a reduced frequency of dysphagia (P 5 .0008). Previous cerebrovascular dis-
ease resulted associated to dysphagia (P 5 .0399). Patients with dysphagia had signif-
icantly lower functional independence measurement (FIM) and level of cognitive
functioning on admission and lower FIM on discharge, longer hospital stay, and
more frequent malnutrition, and they were more frequently aphasic and dysarthric.
Percutaneous endoscopic gastrostomy was used in 18 of 151 patients (11.9%) (41.8%
of patients with VFS-proved dysphagia). Conclusions: Dysphagia occurs in more
than a third of patients with stroke admitted to rehabilitation. Clinical assessment
demonstrates good correlation with VFS. The grade of dysphagia correlates with
dysarthria, aphasia, low FIM, and level of cognitive functioning. Large cortical strokes
of nondominant side are associated with dysphagia. Key Words: Dysphagia—
stroke—videofluoroscopy—percutaneous endoscopic gastrostomy.
Ó 2009 by National Stroke Association

Dysphagia is a disorder of deglutition affecting the oral,
pharyngeal, and/or esophageal phases of swallowing.
Oropharyngeal dysphagia is any abnormality in swallow-
From the *Neurorehabilitation, †Radiology; and ‡Internal Medicine
and Geriatrics Units, Local Health Unit 8, S. Donato Hospital, Arezzo,
Italy.
Received January 1, 2009; accepted January 13, 2009.
Address correspondence to Paolo Falsetti, MD, PhD, Neurorehabi-
litation Unit, Local Health Unit 8, S. Donato Hospital, Arezzo, Italy.
E-mail: paolo.falsetti@virgilio.it.
1052-3057/$—see front matter
Ó 2009 by National Stroke Association
doi:10.1016/j.jstrokecerebrovasdis.2009.01.009
ing physiology of the upper aerodigestive tract and it oc-
curs frequently after stroke, with an incidence ranging
widely between 29% and 81%.1-3 This discrepancy be-
tween studies depends on different methods of diagnosis,
time after stroke, and types of lesion. Aspiration (passage
of material into the larynx below the true vocal cords) af-
ter swallowing, especially fluids, is probably the most se-
vere aspect of oropharyngeal dysphagia with incidence
between 22% and 52%.4-6 Nearly half of aspirations in pa-
tients with stroke are silent7,8 and they have been associ-
ated with increased morbidity and mortality in many
studies.9

Journal of Stroke and Cerebrovascular Diseases, Vol. 18, No. 5 (September-October), 2009: pp 329-335 329
330
Moreover, the presence of oropharyngeal dysphagia in
patients recovering from stroke has often been associated
with malnutrition, dehydration, pulmonary infections,
prolonged hospital stay, and death.10,11 Lower respiratory
tract infection is probably the most severe event related to
dysphagia in the early period after stroke, and it is more
common in patients with oropharyngeal dysphagia and
aspirations.12
The early diagnosis of aspiration should induce clini-
cians to limit oral administration of nutrients or drugs
to reduce the incidence of pulmonary infections. How-
ever, bedside swallowing assessments lack the accuracy
to be used as a screening test in stroke, in particular in pa-
tients with alteration of consciousness.7,13 Moreover, bed-
side prediction of aspiration seems to be inaccurate.8,14,15
Videofluoroscopy (VFS) can be considered as gold stan-
dard in diagnosing dysphagia with aspirations (silent or
not) because of the capability to study the entire process
of deglutiton.16-18 Nevertheless, this examination necessi-
tates patient collaboration and sitting posture, so it cannot
be proposed for all patients in the very early period after
stroke.
In this study we have undertaken a prospective analy-
sis of consecutive patients with stroke in a postintensive
neurorehabilitation unit to define incidence of oropharyn-
geal dysphagia (both by clinical and instrumental
methods), compare clinical bedside assessment and VFS
(considered as gold standard), and define any correlation
between the presence of dysphagia (both clinically and
VFS proved) and clinical characteristic of patients with
stroke (nutritional and functional status, type of stroke,
incidence of pulmonary infections).
Methods
In all, 151 consecutive inpatients admitted to our neuro-
rehabilitation unit between January 2005 and December
2006 with diagnosis of previous ischemic or hemorrhagic
stroke were enrolled in this study. All patients were trans-
ferred to the neurorehabilitation unit after the acute
phase, with a mean length of stay on intensive care unit
of 13 days (range 6-21).
Patients with a history of head and neck damage, his-
tory of neurologic disease other than cerebrovascular dis-
orders, or current dysphagia were excluded from the
study. The ethical committee of the hospital approved
the study.
The characteristics of study participants were: 77 male,
74 female, mean age 79.4 years (range 58-91), and mean
duration of disease (time from stroke) 14 days.
The diagnosis of stroke was always confirmed by com-
puted tomography (CT), magnetic resonance imaging, or
both, and the last scan of each patient was reviewed to
classify the lesion location (Table 1) and to define the
type of stroke (ischemic or hemorrhagic). The presence
of signs of cerebrovascular disease (other than the recent
P. FALSETTI ET AL.
stroke) was recorded and classified (no cerebrovascular
disease, diffuse cerebrovascular disease, previous stroke).
Classification of stroke location was made on the basis of
the damaged area on CT/magnetic resonance imaging in 7
subtypes: cortical stroke on dominant side (generally left);
cortical stroke on nondominant side (generally right);
subcortical stroke on dominant side (generally left);
subcortical stroke on nondominant side (generally right);
brainstem stroke; cerebellar stroke; and mixed/multifocal
stroke. This classification derived from previous radio-
logic and clinical methods of ischemic stroke classifica-
tion19,20 with indication of side location.21 In particular,
cortical stroke corresponds to total or partial anterior circu-
lation stroke of Oxfordshire Community Stroke Project–
derived CT stroke classification, subcortical stroke
corresponds to small partial anterior circulation stroke
(striatocapsular) or lacunar stroke, and brainstem or cere-
bellar stroke corresponds to posterior circulation stroke.19
The patients were enrolled regardless of cognitive func-
tion, consciousness level, grade of collaboration, or capa-
bility of communication. Presence of aphasia (defined as
deficit in at least one of the 4 language areas: comprehen-
sion, fluency, naming, and repetition) and dysarthria
(defined as deficit of articulatory agility of speech) was
recorded for each patient.21
On admission and on discharge each patient underwent
neurologic and functional assessment, even with defini-
tion of functional independence measurement (FIM) score
and level of cognitive functioning (LCF) score.
Nutritional state was assessed by clinical and biochem-
ical parameters on admission and on discharge determin-
ing serum levels of albumin, ferritin, iron, urea, and
lymphocyte count, and weight loss. Malnutrition was
diagnosed when at least 2 of 5 parameters were altered.22
Lower respiratory tract infections (diagnosed with
fever .38 C and abnormal chest radiograph result)
from the time of stroke to discharge were recorded.3,6
A standardized clinical bedside test was performed by
the doctor in each patient within 1 day from admission.
This test was arranged in 3 steps and it was influenced
by previous works6,17,23 and guidelines.10
The first step served to identify the level of conscious-
ness and collaboration of patient (patients with LCF ,4
were immediately considered dysphagic) and to define
oral motor and sensory assessment (voice quality; speech
and language; swallowing of saliva; movements of cricoid
cartilage; lips, tongue, and velopharynx; gag reflex; pres-
ervation of pharyngeal sensation; capability of voluntary
cough).
The second step comprised the swallowing of 5 mL of
water with concomitant pulse oxymetry, carefully observ-
ing signs of oral-facial apraxia (loosening of water from
lips, delay in swallowing, abnormality or absence of
tongue movements) or signs of penetration/aspiration
(‘‘wet’’ or ‘‘gurgly’’ voice, coughing, .2% decrease of
basal value of oxygen saturation at pulse oximetry).
DYSPHAGIA FOLLOWING STROKE 331

Table 1. Demographic and clinical characteristics of patients

Overall study population No dysphagia Dysphagia P value (statistic test)

No. of patients (n) 151 89 (58.9%) 62 (41.0%)

Female (n) 74 43 31 ns (Chi square)
Male (n) 77 46 31 ns (Chi square)
Mean age, y (range; SD) 79.4 (58-91; 6.2) 78.6 (58-87; 6.6) 80.7 (58-91; 5.4) ns (Mann-Whitney)
Mean duration of disease 14 13 15 ns (Mann-Whitney)
(days from stroke)
Type of recent stroke
 Ischemic 112 (74.1%) 65 (73.0%) 47 (75.8%) ns (Chi square)
 Hemorrhagic 39 (25.8%) 24 (26.9%) 15 (24.1%)
Classification of stroke .0251 overall (Chi square)
location
 Cortical stroke- 33 (21.8%) 18 (19.7%) 15 (25%) asp: 3 ns (Fisher)
dominant side (generally
left) TACI or PACI
 Cortical stroke- 35 (23.1%) 15 (16.8%) 20 (32.2%) asp: 5 .0322 (Fisher)
nondominant side
(generally right) TACI or
PACI
 Subcortical stroke- 24 (15.8%) 12 (7.9%) 12 (20%) asp: 4 ns (Fisher)
dominant side (generally
left) striatocapsular-
PACI or LACI
 Subcortical stroke- 30 (19.8%) 26 (28.5%) 4 (6.6%) asp: 0 .0008 (Fisher)
nondominant side
(generally right)
striatocapsular-PACI or
LACI
 Brainstem stroke POCI 16 (10.5%) 8 (8.7%) 8 (13.3%) asp: 0 ns (Fisher)
 Cerebellar stroke POCI 11 (7.2%) 8 (8.7%) 3 (5%) asp: 1 ns (Fisher)
 Mixed or multifocal 2 (1.3%) 2 (2.1%) 0% asp: 0 ns (Fisher)
stroke
Cerebrovascular disease
 No cerebrovascular 17 (11.2%) 14 (15.3%) 3 (5%) .0399 (Fisher: disease v no
disease disease)
 Diffuse cerebrovascular 110 (72.8%) 66 (74.1%) 44 (70.9%)
disease
 Previous stroke 24 (15.8%) 9 (9.8%) 15 (25%) ns (Fisher: diffuse v focal)
LCF at admission (range; 6.3 (3-8; 1.3) 6.7 (4-8; 1.0) 5.7 (3-8; 1.4) ,.0001 (Mann-Whitney)
SD)
FIM (range; SD)
 At admission 45.9 (18-106; 21.6) 53.1 (18-106; 20.1) 35.6 (18-92; 19.6) ,.0001 (Mann-Whitney)
 At discharge 59.6 (18-129; 26.9) 68.5 (19-129; 25) 46.8 (18-122; 24.4) ,.0001 (Mann-Whitney)
Length of stay, days (range; 29.9 (6-93; 14.7) 26.6 (6-60; 12.3) 35 (13-93; 16.7) .0012 (Mann-Whitney)
SD)
Lower respiratory tract 9 (5.9%) 1 (1.1%) 8 (12.9%) .0036 (Fisher)
infection
Malnutrition 132 (87.4%) 73 (82.0%) 59 (95.1%) .0230 (Fisher)
Aphasia 48 (31.7%) 16 (17.5%) 32 (53.3%) ,.0001 (Fisher)
Dysarthria 83 (54.9%) 28 (30.7%) 55 (91.6%) ,.0001 (Fisher)
PEG 18 (11.9%) 0% 18 (30%) ,.0001 (Fisher)

Abbreviations: asp, aspirating at videofluoroscopy; FIM, functional independence measurement; LACI, lacunar infarction; LCF, level of cog-
nitive functioning; ns, not significant; PACI, partial anterior circulation infarction; PEG, percutaneous endoscopic gastrostomy; POCI, posterior
circulation infarction; TACI, total anterior circulation infarction.
332 P. FALSETTI ET AL.

The third step consisted of swallowing at least 20 mL of

water, with the same procedures just described.
On the basis of the results of the 3-step bedside swal-
lowing assessment, each patient was described as dys-
phagic (abnormality of at least one of the items
described in each step) or nondysphagic (complete nor-
mality in each step). Clinically proved dysphagia was
classified in 3 categories (1 5 dysphagia prevalently af-
fecting oral phase, 2 5 dysphagia prevalently affecting
pharyngeal phase, 3 5 mixed dysphagia).
Patients classified as clinically dysphagic were further
evaluated with VFS. VFS was completed with a standard
protocol4,8,24 within the first week of admission. A video-
recording of the oral cavity and pharynx was obtained in
the lateral plane while the patient swallowed in sequence
5 mL and 10 mL of solution of barium of different consis-
tency (liquid at later attempts of the examination). The ex-
aminations were stopped if the patient exhibited
significant aspiration.
VFS-proved dysphagia was classified into 4 categories
(0 5 no dysphagia, 1 5 dysphagia affecting oral phase,
2 5 dysphagia affecting pharyngeal phase, 3 5 mixed
dysphagia). The ordinal penetration-aspiration scale
was used for scoring airway invasion (Figs 1 and 2).25
Statistical analysis was performed with software (InStat 3 Figure 1. Female, 89 years. Patient with left cortical ischemic stroke and
GraphPad, GraphPad Software Inc., LaJolla, CA 92037). The diffuse cerebrovascular disease, right hemiplegia, nonfluent aphasia, apraxia,
Chi-square test was used for an overall approach to compare oropharyngeal dysphagia. VFS demonstrated grade 5 on penetration-aspira-
tion scale (contrast agent contacting vocal folds with visible residue and with-
the percentages among groups. Fisher exact test was used to
out patient response). Decreased capability of oral clearance. Lateral scan.
compare the percentages between two groups. Pearson sta-
tistics and Spearman rank test were applied to correlate vari-
ables (respectively with or without normal distribution). In all, 49 of 151 patients (79% of clinically dysphagic
The level of statistical significance was set at a P level of .05. patients) underwent VFS. Dysphagia prevalently affecting
oral phase was observed in 15, dysphagia prevalently af-
fecting pharyngeal phase was observed in 13, and mixed
Results
form of dysphagia was observed in 15. Six patients clini-
The patients were admitted with a mean LCF of 6.31 cally suggested to be dysphagic had a normal VFS result.
(range 3-8) and FIM of 45.9 (range 18-106). Mean FIM at Spearman correlation between clinical and VFS diagnosis
discharge was 59.6 (range 18-129), with a mean increment of dysphagia was highly significant (r 5 0.6505, P ,.0001).
of 13.7. The mean length of stay on neurorehabilitation Penetrations were observed in 21 of 49 patients (42.8%).
unit was 29.9 days (range 6-93). Aspirations were observed in 13 of 49 patients (26.5%)
Imaging techniques demonstrated no previous cerebro- and in 6 cases (12.2%) were classified as silent and signif-
vascular disease in 17 of 151 patients, diffuse cerebrovas- icant.
cular disease in 110 of 151, and a previous stroke in 24 of The diagnosis of dysphagia was not influenced by type
151. The prevalence of lesion location of the recent stroke of stroke. Instead, stroke location and side showed signif-
is reported in Table 1. The type of stroke was ischemic in icant association with dysphagia (Table 1). In particular,
112 patients and hemorrhagic in 39. cortical stroke of nondominant side showed more fre-
Aphasia was observed in 48 patients (31.7%) and dysar- quent dysphagia (P 5 .0322). On the other hand, subcorti-
thria in 83 (54.9%). Biochemical diagnosis of malnutrition cal nondominant stroke showed a reduced frequency of
was made in 132 patients (87.4%). dysphagia (P 5 .0008). In addition, the presence of previ-
Dysphagia was clinically diagnosed in 62 of 151 pa- ous cerebrovascular damage (indifferent if focal or dif-
tients (41%). Five patients (3.3%) were considered dys- fuse) was associated with dysphagia (P 5 .0399).
phagic without clinical testing because of their low Lower respiratory tract infections until discharge were
awareness level (LCF , 4) on admission. observed in 9 of 151 patients (5.9%) and they were signif-
Dysphagia prevalently affecting oral phase was ob- icantly more frequent in those with dysphagia (P 5.0036).
served in 23 patients, dysphagia prevalently affecting pha- Dysphagic patients also had lower LCF on admission
ryngeal phase in 14, and mixed form of dysphagia in 25. (P , .0001) and discharge (P , .0001), longer hospital
DYSPHAGIA FOLLOWING STROKE
Figure 2. Female, 86 years. Patient with right cortical ischemic stroke, left
hemiplegia, hemispatial neglect, and oropharyngeal dysphagia. VFS demon-
strated grade 8 on penetration-aspiration scale (contrast agent passing glot-
tis; visible subglottic residue without patient response). Anteroposterior
scan.
stay (P 5 .0012), and more frequent malnutrition (P 5
.023), and they were more frequently aphasic and dys-
arthric (P , .0001).
Spearman analysis showed significant direct correlation
between the grade of clinically proved dysphagia and dys-
arthria (r 5 0.2962, P 5 .0002), aphasia (r 5 0.3553, P ,
.0001), and inverse correlation with FIM (r 5 –0.2925, P
5 .0287) and LCF (r 5 –0.3383, P 5 .0082) at admission.
Percutaneous endoscopic gastrostomy (PEG) was used
in 18 of 151 patients (11.9%; 41.8% of 43 patients with VFS-
proved dysphagia).
Correlation analysis showed significant direct correla-
tion between PEG and grade of aspiration at VFS (r 5
0.4339, P 5 .0015), aphasia (r 5 0.5482, P , .0001), and
length of rehabilitation hospital stay (r 5 0.3189, P 5
.0115), and inverse correlation with FIM (r 5 –0.4969,
P , .0001) and LCF (r 5 –0.4893, P , .0001) at admission
and improvement of FIM score at discharge (r 5 –0.3622,
P 5 .0061).
Discussion
Dysphagia is a common complication after stroke, but
its prevalence is widely discrepant in the various studies,
ranging between 29%1 and 81%.2,3 The frequency of
dysphagia in rehabilitation studies ranges widely
333
26 2
between 25% and 81%. These prevalences are probably
dependent on which method is used for the diagnosis, the
time from stroke, and the severity of stroke in the case
study.
The results of this study have been derived from a hos-
pital-referred cohort of consecutive patients with stroke
admitted to a neurorehabilitation unit. The timing of the
assessment and the diagnostic methods could have deter-
mined some bias in the results with respect to similar
studies.
Our results confirm that dysphagia occurs in more than
a third (41%) of consecutive patients with stroke admitted
to a neurorehabilitation unit. Feeding gastrostomy tubes
(PEG) were inserted in 11.9% of our neurorehabilitation
population. The percentage of severe dysphagic stroke re-
quiring PEG is comparable with previous neurorehabili-
tation studies.27 A direct correlation was observed
between insertion of PEG and aphasia, aspiration at
VFS, and length of rehabilitation hospital stay, and an in-
verse correlation with FIM and LCF at admission, and im-
provement of FIM score at discharge. A previous
rehabilitation study confirmed significant lower FIM
scores in patients with stroke who require PEG placement
for the management of dysphagia and not significant dif-
ferences in FIM improvement and length of hospital stay
in these patients.28
In our study 79% of clinically dysphagic patients under-
went VFS. Six patients clinically suggested to be dysphagic
had a normal VFS finding. However, the clinical classifica-
tion of dysphagia showed good correlation with VFS.
A comparison with the previous study of Smithard
et al13 in patients with acute stroke shows a low sensibility
(47%) of bedside assessment in predicting aspiration.
However, in our study the diagnosis of dysphagia com-
prised even oral phase alterations, and not only aspira-
tions. This could probably increase the prevalence of
clinical dysphagia and subsequently improve the sensi-
tivity of bedside assessment with regard to VFS.
Therefore, clinical bedside assessment is a necessary
screening test, with high correlation with VFS. However,
criteria that is too wide for clinical diagnosis of dysphagia
could generate false-positive findings, as in our case
study.
Lower respiratory tract infections were observed in
5.9% of patients. The pneumonia incidence in our study
is lower than in previous rehabilitation studies, where it
ranged widely between 7% and 29%.26,29,30 Nevertheless,
in patients with dysphagia, pneumonia was diagnosed
with significantly higher frequency.
A direct correlation was observed between grade of
dysphagia and dysarthria and aphasia, and inverse corre-
lation was observed with FIM and LCF at admission.
Moreover, in the dysphagic group, significantly longer
length of stay, frequency of malnutrition, and lower FIM
and LCF have been observed. These correlations were
observed in previous work.10,27
334
The association between aphasia and dysphagia was
observed by Barer,1 whereas in a more recent study
Schroeder et al21 underlined that hemispatial neglect
shows a stronger association with dysphagia than apha-
sia. In our study we did not consider hemispatial neglect
as an independent variable.
However, in our case study cortical stroke of nondom-
inant side showed significantly higher prevalence of dys-
phagia, in contrast to subcortical nondominant stroke that
was significantly not associated with dysphagia. As hemi-
spatial neglect is characteristically associated to cortical
right (nondominant) hemispheric damage but not associ-
ated to internal capsule (subcortical) and lacunar right-
sided damage,21,31 our results indirectly confirm those
of Schroeder et al.21 Other studies confirmed that right
hemisphere lesions are associated to dysphagia with aspi-
rations.32,33
No other correlation was observed in our study be-
tween dysphagia and location or type of stroke. This find-
ing was consistent with results from previous studies,21,34
and our lesion mapping in patients with stroke undergo-
ing rehabilitation has not indicated differences in swal-
lowing dysfunction (oral dysmotility, pharyngeal
dysfunction, penetration, aspiration) with different loca-
tion or type of lesion.
Several studies indicated that large cortical hemi-
spheric lesions (with or without indication of side) dem-
onstrate the highest incidence of dysphagia.33,35-38 Our
results demonstrate significantly higher incidence of dys-
phagia only for right cortical strokes. However, the corre-
lations between dysphagia and aphasia and dysarthria
indirectly confirm the importance of left cortical hemi-
spheric lesions. The correlation with low scores of FIM
and LCF could indirectly indicate that large and more se-
vere lesions can increase the incidence of dysphagia.36,37
Posterior circulation strokes were also not associated
with dysphagia in our study. This finding is incongruent
with previous studies that identified severe dysphagia in
patients with stroke and brainstem lesions.2,30,39 On the
other hand, many studies confirmed that brainstem and
cerebellar stroke are not significantly associated with
higher prevalence of dysphagia.35-37,40-42
However, in our study only 16 patients had brainstem
lesions and we did not identify precise lesion location.
This could have reduced the statistical significance on
this subgroup.
Thus, whether lesion size, location, or type of stroke in
conjunction with clinical or neurocognitive defects are re-
lated to dysphagia and aspiration remains debated and
further study is needed to clarify this question.
References
1. Barer DH. The natural history and functional conse-
quences of dysphagia after hemispheric stroke. J Neurol
Neurosurg Psychiatry 1989;52:236-241.
P. FALSETTI ET AL.
2. Meng NH, Wang TG, Lien IN. Dysphagia in patients with
brainstem stroke: Incidence and outcome. Am J Phys
Med Rehabil 2000;79:170-175.
3. Martino R, Foley N, Bhogal S, et al. Dysphagia after
stroke: Incidence, diagnosis, and pulmonary complica-
tions. Stroke 2005;36:2756-2763.
4. Kidd D, Lawson J, Nesbitt R, et al. Aspiration in acute
stroke: A clinical study with videofluoroscopy. QJM
1993;86:825-829.
5. Lim SH, Lieu PK, Phua SY, et al. Accuracy of bedside clin-
ical methods compared with fiberoptic endoscopic exam-
ination of swallowing (FEES) in determining the risk of
aspiration in acute stroke patients. Dysphagia 2001;
16:1-6.
6. Mann G, Hankey GJ, Cameron D. Swallowing function
after stroke: Prognosis and prognostic factors at 6
months. Stroke 1999;30:744-748.
7. Terré R, Mearin F. Oropharyngeal dysphagia after the
acute phase of stroke: Predictors of aspiration. Neurogas-
troenterol Motil 2006;18:200-205.
8. Splaingard ML, Hutchins B, Sulton LD, et al. Aspirations
in rehabilitation patients: Videofluoroscopy vs bedside
clinical assessment. Arch Phys Med Rehabil 1988;
69:637-640.
9. Ramsey D, Smithard D, Kalra L. Silent aspiration: What
do we know? Dysphagia 2005;20:218-225.
10. Martino R. Preferred practice guideline for dysphagia
2000. Available from: URL:http://www.caslpo.com/
english_site/DYSPHAGIADOCUMENT.pdf. Accessed
February 14, 2007.
11. Crary MA, Carnaby-Mann GD, Miller L, et al. Dysphagia
and nutritional status at the time of hospital admission
for ischemic stroke. J Stroke Cerebrovasc Dis 2006;
15:164-171.
12. Kidd D, Lawson J, Nesbitt R, et al. The natural history
and clinical consequences of aspiration in acute stroke.
QJM 1995;88:409-413.
13. Smithard DG, O’Neill PA, Park C, et al. Can bedside as-
sessment reliably exclude aspiration following acute
stroke? Age Ageing 1998;27:99-106.
14. Linden P, Siebens AA. Dysphagia: Predicting laryngeal
penetration. Arch Phys Med Rehabil 1983;64:281-284.
15. Linden P, Kuhlemeyer KV, Paterson C. The probability of
correctly predicting subglottic penetration from clinical
observations. Dysphagia 1993;8:170-179.
16. Horner J, Massey EW. Silent aspiration following stroke.
Neurology 1988;38:317-319.
17. Smith HA, Lee SH, O’Neill PA, et al. The combination of
bedside swallowing assessment and oxygen saturation
monitoring of swallowing in acute stroke: A safe and hu-
mane screening tool. Age Ageing 2000;29:495-499.
18. Ramsey D, Smithard DG, Kalra L. Early assessment of
dysphagia and aspiration risk in acute stroke patients.
Stroke 2003;34:1252-1257.
19. Smith CJ, Emsley HC, Libetta CM, et al. The Oxfordshire
community stroke project classification in the early hours
of ischemic stroke and relation to infarct site and size on
cranial computed tomography. J Stroke Cerebrovasc Dis
2001;10:205-209.
20. Bamford J, Sandercock P, Dennis M, et al. Classification
and natural history of clinically identifiable subtypes of
cerebral infarction. Lancet 1991;337:1521-1526.
21. Schroeder MF, Daniels SK, McClain M, et al. Clinical and
cognitive predictors of swallowing recovery in stroke.
J Rehabil Res Dev 2006;43:301-310.
22. Finestone HM, Greene-Finestone LS, Wilson ES, et al.
Malnutrition in stroke patients on the rehabilitation
DYSPHAGIA FOLLOWING STROKE
service and at the follow-up: Prevalence and predictors.
Arch Phys Med Rehabil 1995;76:310-316.
23. Daniels SK, Schroeder MF, McClain M, et al. Dysphagia
after stroke: Development of a standard method to exam-
ine swallowing recovery. J Rehabil Res Dev 2006;
43:347-356.
24. Gates J, Hartnell GG, Gramigna GD. Videofluoroscopy
and swallowing studies for neurologic disease: A primer.
Radiographics 2005;26:e22.
25. Rosenbek JC, Robbins JA, Roecker EB, et al. A penetra-
tion-aspiration scale. Dysphagia 1996;11:93-98.
26. Gottlieb D, Kipnis M, Sister E, et al. Validation of the 50
mL 3 drinking test for evaluation of post-stroke dyspha-
gia. Disabil Rehabil 1996;18:529-532.
27. Ickenstein GW, Stein J, Ambrosi D, et al. Predictors of sur-
vival after severe dysphagic stroke. J Neurol 2005;
252:1510-1566.
28. Iizuka M, Reding M. Use of percutaneous endoscopic
gastrostomy feeding tubes and functional recovery in
stroke rehabilitation: A case-matched controlled study.
Arch Phys Med Rehabil 2005;86:1049-1052.
29. DePippo KL, Holas MA, Reding MJ. The burke dyspha-
gia screening test: Validation of its use in patients with
stroke. Arch Phys Med Rehabil 1996;75:1284-1286.
30. Chua KSG, Kong KH. Functional outcome in brainstem
stroke patients after rehabilitation. Arch Phys Med Reha-
bil 1996;77:194-197.
31. Goldstein LB, Jones MR, Matchar DB, et al. Improving the
reliability of stroke subgroup classification using the trial
of ORG 10172 in acute stroke treatment (TOAST) criteria.
Stroke 2001;32:1091-1097.
335
32. Smithard DG, O’Neill PA, Martin DF, et al. Aspiration fol-
lowing stroke: Is it related to the side of the stroke? Clin
Rehabil 1997;11:73-76.
33. Daniels SK, Foundas AL, Iglesia GC, et al. Lesion site in
unilateral stroke patients with dysphagia. J Stroke Cere-
brovasc Dis 1996;6:30-34.
34. Alberts MJ, Horner J, Gray L, et al. Aspiration after
stroke: Lesion analysis by brain MRI. Dysphagia 1992;
7:170-173.
35. Langdon PC, Lee AH, Binns CW. Dysphagia in acute is-
chemic stroke: Severity, recovery and relationship to
stroke subtype. J Clin Neurosci 2007;14:630-634.
36. Broadley S, Croser D, Cottrel J, et al. Predictors of pro-
longed dysphagia following acute stroke. J Clin Neurosci
2003;10:300-305.
37. Paciaroni M, Mazzotta G, Corea F, et al. Dysphagia fol-
lowing stroke. Eur Neurol 2004;51:162-167.
38. Barros AF, Fabio SR, Furkim AM. Relation between clin-
ical evaluation of deglutition and computed tomography
in acute ischemic stroke patients. Arq Neuropsiquiatr
2006;64:1009-1014.
39. Kim H, Chung CS, Lee KH, et al. Aspirations subsequent
to a pure medullary infarction: Lesion sites, clinical vari-
ables and outcome. Arch Neurol 2000;57:478-483.
40. Daniels SK, Foundas AL. Lesion localization in acute
stroke patients with risk of aspiration. J Neuroimaging
1999;9:91-98.
41. Lawrence ES, Coshall C, Dundas R, et al. Estimates of the
prevalence of acute stroke impairments and disability in
a multiethnic population. Stroke 2001;32:1279-1284.
42. Terao S, Miura N, Osano Y, et al. Multiple cerebellar in-
farcts: Clinical and pathophysiologic features. J Stroke
Cerebrovasc Dis 2005;14:193-198.